乌司他丁对小鼠内毒素性急性肺损伤的保护作用

Protective Effection of Ulinastatin on Acute Lung Injury Induced by Endotoxin in Mice

目的探讨乌司他丁(UTI)对内毒素性急性肺损伤的保护作用及其机制。方法将昆明种小鼠50只随机分为脂多糖(LPS)组和UTI组,腹腔注射LPS建立小鼠急性肺损伤模型,直接心脏穿刺抽血查血气分析,用放射免疫法分别测定各组各时相点肺组织匀浆上清液中肿瘤坏死因子α(TNF-α)、白介素-8(IL-8)、白介素-10(IL-10)3种细胞因子的含量,同时观察肺组织形态学改变,进行肺湿/干重比值(W/D)测定。结果两组小鼠肺组织中炎症因子呈明显上升趋势,UTI组促炎因子升高幅度显著低于LPS组(P<0.01),而抗炎因子升高幅度明显高于LPS组(P<0.05),且肺组织W/D值明显低于LPS组(P<0.05),血氧分压(PaO2)高于LPS组(P<0.05)。结论UTI可减轻炎症因子介导的急性肺损伤,其机制可能是通过调节促炎因子/抗炎因子平衡来实现的。

Objective To investigate the protective effect of ulinastatin on LPS- induced acute lung injury and its possible mechanism. Methods Fifty mice were randomly divided into 2 groups：LPS group and UTI group. The ALI model was set up by intraperineal injection of lipopolysaccharide（LPS）. Blood samples were taken through heart puncture for blood gas analysis. The choalges of TNF-α,IL-8,IL-10 levels in the pulmonary tissues were detected by ELISA at defferent times. Besides, the following changes were observed：lung wet/dry weight ratio,lung histological manifestations. Results The levels of inflammatory factors in two groups mice all took on a ascending trend. TNF-α,IL-8 and W/D levels were lower significantly in UTI group than those in LPS group（P〈0.05）. However,IL- 10 and PaO2 levels were higher obviously in UTI group than those in LPS group（P〈0. 05）. Conclusion UTI can lessen the acute lung injury induced by inflammatory factors,which may be the mechanism through regulating the balance of pro- inflammatory factor/anti- inflammatory factor.